In classical cardiac electrophysiology much attention has been directed at characterizing patterns of frequent ventricular ectopic beat activity. Examples include description of bigeminal rhythms in which there is an alternation between supraventricular and ectopic beats, trigeminy in which there is a sequence of two supraventricular beat and one ectopic beat, as well as many variants (Schulte-Frohlinde V et al., Phys Rev E Stat Nonlin Soft Matter Phys, 2002, 66(3 Pt 1), 031901). Since frequent premature ventricular complexes (PVCs) often precede a sustained ventricular arrhythmia (Bardy G H et al., Zipes D P, Jalife J, eds, Cardiac Electrophysiology: From Cell to Bedside, Philadelphia, Pa.: WB Sauders Co., 1990, 778-90; Bayes de Luna A et al., Am Heart J, 1989, 117(1), 151-9; El-Sherif N et al., J Am Coll Cardiol 1999, 33(5), 1415-23; Kempf F C Jr et al., Am J Cardiol, 1984, 53(11), 1577-82; Lewis B H et al., J Am Coll Cardiol, 1983, 2(3), 426-36; Locati E H et al., J Am Coll Cardiol, 1995, 25(7), 1564-75; Maia I G et al., Rev Port Cardiol, 1993, 12(2), 163-8), researchers initially hypothesized that drugs that suppressed ventricular ectopy would reduce the incidence of sudden cardiac death in high risk patients. However, many classes of drugs, including those that suppress PVCs, have proarrhythmic effects. Furthermore, the analysis of the patterns of ectopy has not provided useful or consistent markers of risk.